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anti-Human SOCS3 Antikörper:
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Human Polyclonal SOCS3 Primary Antibody für ELISA, IF (p) - ABIN670416
Liu, Ao, Zhou, Cui, Zhou, Yuan, Xiang, Cao, Liu: CpG island hypermethylation of multiple tumor suppressor genes associated with loss of their protein expression during rat lung carcinogenesis induced by 3-methylcholanthrene and diethylnitrosamine. in Biochemical and biophysical research communications 2010
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Human Monoclonal SOCS3 Primary Antibody für ELISA, WB - ABIN2476543
Rychlíková, Démant: Influence of non-H-2 genotype on the response to H-2-linked mixed lymphocyte reaction stimulating (MLR-S) genes. in Folia biologica 1975
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Human Polyclonal SOCS3 Primary Antibody für IHC, IHC (p) - ABIN4355049
Harris, Apolzan: Hexosamine biosynthetic pathway activity in leptin resistant sucrose-drinking rats. in Physiology & behavior 2014
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Human Polyclonal SOCS3 Primary Antibody für IHC (p), WB - ABIN3044272
Wan, Che, Kang, Wu: SOCS3 blocks HIF-1? expression to inhibit proliferation and angiogenesis of human small cell lung cancer by downregulating activation of Akt, but not STAT3. in Molecular medicine reports 2015
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Human Polyclonal SOCS3 Primary Antibody für WB - ABIN1883384
Kim, Kim, Liu, Cao, Chen: Regulation of interleukin-6-induced hepatic insulin resistance by mammalian target of rapamycin through the STAT3-SOCS3 pathway. in The Journal of biological chemistry 2008
Human Monoclonal SOCS3 Primary Antibody für IF, IHC (p) - ABIN522456
Pierconti, Martini, Pinto, Cenci, Capodimonti, Calarco, Bassi, Larocca: Epigenetic silencing of SOCS3 identifies a subset of prostate cancer with an aggressive behavior. in The Prostate 2011
Dog (Canine) Polyclonal SOCS3 Primary Antibody für ELISA, WB - ABIN546695
Roberts, Robb, Rakar, Hartley, Cluse, Nicola, Metcalf, Hilton, Alexander: Placental defects and embryonic lethality in mice lacking suppressor of cytokine signaling 3. in Proceedings of the National Academy of Sciences of the United States of America 2001
Polyclonal SOCS3 Primary Antibody für IHC (fro), IP - ABIN541100
Orr, Morgan, Buick, Boyd, Elliott, Burrows, Jefferies, Crocker, Johnston: SOCS3 targets Siglec 7 for proteasomal degradation and blocks Siglec 7-mediated responses. in The Journal of biological chemistry 2007
Mouse (Murine) Polyclonal SOCS3 Primary Antibody für IHC, WB - ABIN3021100
Zou, Liao, Fu, Zhao, Chen, Zhang: MicroRNA-30c-5p ameliorates hypoxia-reoxygenation-induced tubular epithelial cell injury via HIF1α stabilization by targeting SOCS3. in Oncotarget 2017
Human Monoclonal SOCS3 Primary Antibody für WB - ABIN94467
Neuwirt, Puhr, Cavarretta, Mitterberger, Hobisch, Culig: Suppressor of cytokine signalling-3 is up-regulated by androgen in prostate cancer cell lines and inhibits androgen-mediated proliferation and secretion. in Endocrine-related cancer 2007
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we report the surprising finding that zebrafish respond to optic nerve lesion by inducing the expression of Sfpq and Socs3a
stat3/socs3 pathway is a key response in all tissue regeneration in zebrafish.
Trpm7 regulates exocrine pancreatic development via the Mg(2+)-sensitive Socs3a pathway.
SOCS3 expression in response to trauma is unaffected by blockade of the mitogen-activated protein kinase pathway by chemical inhibitors
The suppressor of cytokine signaling 3 gene was identified in this species, and the base sequence and deduced amino acid sequence are presented.
in homozygotes, GH signaling is reduced by the action of the SOCS1 and SOCS3 proteins.
MiR-221 decreases proliferation potency of PANC-1 cells and affects JAK-STAT3 signaling pathway via inhibiting SOCS3.
The SOCS3 gene is significantly associated with the development of lumbar adolescent idiopathic scoliosis in Chinese population.
Our results underline the importance of the functional SOCS3 polymorphisms in the modulation of CHC progression and suggest their contribution to HCC development by affecting its mRNA expression and perturbing key metabolic parameters.
SOCS3 overexpression rescued the IL-9-induced effects. Altogether, IL-9 participates in the pathogenesis of Ulcerative colitis (UC) through STAT3/SOCS3 signaling pathway and has the potential to serve as a possible therapeutic candidate in patients with UC
A group of activator protein-1-related genes were highly up-regulated in Socs3 cKO mice of both ages. This observation was validated using qRT-PCR by SOCS3-depleted human keratinocyte-derived HaCaT cells. Our results suggest that, in addition to participating in immune-mediated pathways, SOCS3 also plays important roles in skin barrier homeostasis.
IL-6, TNF-alpha production, SOCS3 mRNA expression were downregulated, while miR-196b-5p and STAT3 mRNA expression were upregulated in monocytes from long-term cigarette smoking-related pulmonary tuberculosis patients as compared to nonsmoking pulmonary tuberculosis patients.
we found key statistical differences for the proteins SEL1, Notch3 and SOCS3 in the progression of uterine cervical cancer
The level of SCOS3 was significantly downregulated SOCS3 in diabetic cardiomyopathy.
SOCS1/3-mediated degradation of IFN regulatory factor 7 directly regulates TLR7 signaling and type I IFN production in pDCs.
The expression of SOCS3 in peripheral blood mononuclear cells and liver tissues of non-responding CHB[ chronic hepatitis B] patients was significantly higher than that of responding CHB patients during interferon and nucleoside antiviral therapy. We speculated that SOCS3 might affect the antiviral efficacy through negative regulation of JAK-STAT signaling pathway, and partly expose the mechanism of interferon resistance.
TGF-beta1 can downregulate the mRNA expression of SOCS-3 and upregulate the mRNA expression of SREBP-1c.
SOCS3 is highly tyrosine phosphorylated by c-Abl and that tyrosine phosphorylation of SOCS3 is required for the survival and tumorigenesis of certain cells. Our findings provide novel insights into complicated mechanisms underlying the oncogenic function of Abl kinases.
In vitro significance of SOCS-3 and SOCS-4 and potential mechanistic links to wound healing have been presented.
Loss or reduced levels of SOCS3 have been linked to cancer-associated inflammation and suppressive immunity leading to enhanced breast tumor growth lung metastasis.
BORIS plays a role in epigenetic regulation of SOCS3 gene promoter methylation and histone methylation in hepatocellular carcinoma.
Downregulation of miR-340 inhibited GC cell proliferation, arrested cell cycle, and facilitated apoptosis through upregulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.
Low SOCS3 expression is associated with higher grade breast cancer.
Low SOCS3 expression is associated with invasion and lymph node metastasis in gastric cancer.
Results show the CAT haplotype in SOCS3 was associated with metabolic syndrome (MetS) in Mexican Mestizos, and type 2 diabetes in Mexican Amerindians.
SOCS3 overexpression decreased JAK-STAT3 signaling pathway activity, declined Bcl-2 expression, inhibited cell proliferation, elevated cell apoptosis, and enhanced Adriamycin sensitivity in T24 cells
In porcine circovirus type 2 subclinical infection, SOCS3 interacted with STAT3 and TNF receptor-associated factor 2, suggesting mechanisms by which SOCS3 inhibits IL-6 and TNF-alpha signaling.
SOCS3 is an important negative regulator of insulin signaling in porcine adipocytes.
mapping to chromosome 12
Low SOCS3 expression is required for milk synthesis and proliferation of dairy cow mammary epithelial cells in vitro.
Monocytes obtained from cows with subclinical infection with MAP had upregulated expression of IL-10 and SOCS-3, which may have attenuated the capacity of mononuclear phagocytes to initiate inflammatory and adaptive immune responses.
The results reveal that SOCS3 is involved in IL23-induced spondyloarthritis and acts as a key regulator of osteoblast differentiation, and suggest that SOCS3 knockdown TG mice may be an ideal animal model for further studies of spondyloarthritis.
miR-30d-mediated direct suppression of SOCS3 acts to protect pancreatic beta-cell functions through the JNK signaling pathway
Aortic dissection development is preceded by focal medial rupture, in which macrophage Socs3 maintains proper inflammatory response and differentiation of smooth muscle cells, thus promoting fibrotic healing to prevent tissue destruction and AD development.
MBD2-mediated Th17 differentiation in severe asthma is associated with impaired SOCS3 expression.
It is a negative feedback inhibitor of cytokine signaling with T-cell-mediated immunosuppressive effects on obliterative bronchiolitis.
SOCS3 critically controls the phenotype and function of macrophages and neutrophils under inflammatory conditions and loss of SOCS3 promotes the angiogenic phenotype of the cells through up-regulation of arginase-1.
SOCS3 impacts on IEC turnover following T. muris infection, potentially through enhancement of IDO. IDO may dampen the immune response which can drive intestinal epithelial cell hyperproliferation in the absence of SOCS3, demonstrating the intricate interplay of immune signals regulating mucosal homeostasis, and suggesting a novel tumour suppressor role of SOCS3.
The findings of this indicated that co-deletion of PTEN and SOCS3 results in modest but measureable enhancement of early regeneration of DRG axons following crush injury.
Our findings suggest a role for murine cytomegalovirus (MCMV)-related stimulation of SOCS1 and SOCS3 in the progression of retinal disease during ocular, but not systemic, MCMV infection.
Lentivirusmediated overexpression of SOCS3 was revealed to ameliorate neutrophilic airway inflammation by inhibiting pulmonary Th17 responses in mice with chronic Pseudomonas aeruginosa lung infections.
These data demonstrate that loss of SOCS3 in cardiomyocytes promotes deoxycorticosterone-acetate -salt-induced cardiac remodeling and inflammation.
In the present study, we investigated the hypothesis that SOCS3 expression in the VMH could exert an important role regulating the metabolic changes typically observed during pregnancy and lactation.
SOCS3 was targeted by miR30a- 5p in allergic rhinitis
SOCS3 was upregulated in lung CD4+ T cells in a mouse model of chronic PA lung infection and exogenous SOCS3 suppressed Th17-mediated neutrophil recruitment in vitro.
findings show SOCS3 does not appear to mediate the early inflammatory or leucine-induced changes in protein synthesis in skeletal muscle
The strength of long bones is determined by coalescence of trabeculae during corticalization.This process is regulated by SOCS3 via a mechanism dependent on IL-6 and expression of sex hormones.
High SOCS3 expression is associated with glioma.
Mechanistic analysis indicated that E47 activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 expression. These findings demonstrate that the balance of Id3 and E47 controls the maintenance of Foxp3 expression in Treg cells and, thus, contributes to Treg cell plasticity.
Our results show, for the first time, that SOCS-3 regulates leptin-induced responses in cartilage
This gene encodes a member of the STAT-induced STAT inhibitor (SSI), also known as suppressor of cytokine signaling (SOCS), family. SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of this gene is induced by various cytokines, including IL6, IL10, and interferon (IFN)-gamma. The protein encoded by this gene can bind to JAK2 kinase, and inhibit the activity of JAK2 kinase. Studies of the mouse counterpart of this gene suggested the roles of this gene in the negative regulation of fetal liver hematopoiesis, and placental development.
suppressor of cytokine signaling 3
, suppressor of cytokine signaling 3a
, STAT-induced STAT inhibitor 3
, cytokine-inducible SH2 protein 3
, cytokine signaling suppressor
, E2a-Pbx1 target gene in fibroblasts 10
, cytokine inducible SH2-containing protein 3
, suppressors of cytokine signaling 3